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| 1 | Cropland redistribution to marginal lands undermines environmental sustainability显示文摘Cropland redistribution to marginal land has been reported worldwide;however,the resulting impacts on environmental sustainability have not been investigated sufficiently.Here we investigated the environmental impacts of cropland redistribution in China.As a result of urbanization-induced loss of high-quality croplands in south China(~8.5 t ha^(-1)),croplands expanded to marginal lands in northeast(~4.5 t ha^(-1)) and northwest China(~2.9 t ha^(-1)) during 1990-2015 to pursue food security.However,the reclamation in these low-yield and ecologically vulnerable zones considerably undermined local environmental sustainability,for example increasing wind erosion(+3.47%),irrigation water consumption(+34.42%),fertilizer use(+20.02%) and decreasing natural habitats(-3.11%).Forecasts show that further reclamation in marginal lands per current policies would exacerbate environmental costs by 2050.The future cropland security risk will be remarkably intensified because of the conflict between food production and environmental sustainability.Our research suggests that globally emerging reclamation of marginal lands should be restricted and crop yield boost should be encouraged for both food security and environmental benefits. | Wenhui Kuang Jiyuan Liu Hanqin Tian Hao Shi Jinwei Dong Changqing Song Xiaoyong Li Guoming Du Yali Hou Dengsheng Lu Wenfeng Chi Tao Pan Shuwen Zhang Rafiq Hamdi Zherui Yin Huimin Yan Changzhen Yan Shixin Wu Rendong Li Jiuchun Yang Yinyin Dou Wenbin Wu Liqiao Liang Bao Xiang Shiqi Yang | 2022 | National Science Review2022，9，1： | 13 |
| 2 | MEF2C promotes M1 macrophage polarization and Th1 responses显示文摘The polarization of macrophages to the M1 or M2 phenotype has a pivotal role in inflammation and host defense;however,the underlying molecular mechanism remains unclear.Here,we show that myocyte enhancer factor 2 C(MEF2C)is essential for regulating M1 macrophage polarization in response to infection and inflammation.Global gene expression analysis demonstrated that MEF2C deficiency in macrophages downregulated the expression of M1 phenotypic markers and upregulated the expression of M2 phenotypic markers.MEF2C significantly promoted the expression of interleukin-12 p35 subunit(Il12a)and interleukin-12 p40 subunit(Il12b).Myeloid-specific Mef2c-knockout mice showed reduced IL-12 production and impaired Th1 responses,which led to susceptibility to Listeria monocytogenes infection and protected against DSS-induced IBD in vivo.Mechanistically,we showed that MEF2C directly activated the transcription of Il12a and Il12b.These findings reveal a new function of MEF2C in macrophage polarization and Th1 responses and identify MEF2C as a potential target for therapeutic intervention in inflammatory and autoimmune diseases. | Xibao Zhao Qianqian Di Han Liu Jiazheng Quan Jing Ling Zizhao Zhao Yue Xiao Han Wu Zherui Wu Wengang Song Huazhang An Weilin Chen | 2022 | Cellular & Molecular Immunology2022，19，4： | 4 |
| 3 | Bioresponsive cisplatin crosslinked albumin hydrogel served for efficient cancer combination therapy显示文摘Combination therapy is one of the potential strategies for tackling complicated tumor treatments like drug resistance.In this work,we have generated a therapeutic cisplatin-crosslinked albumin hydrogel(BC-Gel)that allows the local release of L-Buthionine-sulfoximine(BSO),cisplatin,and glucose oxidase(GOx)with distinct release kinetics.The BC-Gel with favorable biostimuli degradability and injectability could release therapeutic agents in a programmed manner within the tumor microenvironment(TME).The preferentially released BSO significantly suppressed the glutathione(GSH)-related cisplatin resistance and sensitized the tumor cells to cisplatin by inhibiting theγ-glutamylcysteine synthetase.Meanwhile,cisplatin achieved a sequential release and long-term treatment following the bioresponsive gel degradation under the combined action of chloride ions(Cl−)and proteinase in the body.In addition,the overproduced H_(2)O_(2)of GOx-catalyzed glucose oxidation accelerated the depletion of existed GSH within cells and further weakened the cisplatin resistance,achieving enhanced tumor treatment together with a strong cell-killing effect.The above sequential drug release strategy based on the dual GSH depletion effect breaks the balance of the GSH-mediated redox TME and enhances the sensitivity of A549 cells to cisplatin forcefully,and provides a promising way for temporal control of drug release as well as efficient cancer combination therapy. | An Yan Zherui Zhang Jiamei Gu Xiaoran Ding Yongchen Chen Jingjing Du Shu Wei Hongcheng Sun Jiayun Xu Shuangjiang Yu Junqiu Liu | 2023 | Nano Research2023，16，2： | 1 |
| 4 | Degradation of FAK-targeting by proteolytic targeting chimera technology to inhibit the metastasis of hepatocellular carcinoma显示文摘Liver cancer is a prevalent malignant cancer,ranking third in terms of mortality rate.Metastasis and recurrence primarily contribute to the high mortality rate of liver cancer.Hepatocellular carcinoma(HCC)has low expression of focal adhesion kinase(FAK),which increases the risk of metastasis and recurrence.Nevertheless,the efficacy of FAK phosphorylation inhibitors is currently limited.Thus,investigating the mechanisms by which FAK affects HCC metastasis to develop targeted therapies for FAK may present a novel strategy to inhibit HCC metastasis.This study examined the correlation between FAK expression and the prognosis of HCC.Additionally,we explored the impact of FAK degradation on HCC metastasis through wound healing experiments,transwell invasion experiments,and a xenograft tumor model.The expression of proteins related to epithelial-mesenchymal transition(EMT)was measured to elucidate the underlying mechanisms.The results showed that FAK PROTAC can degrade FAK,inhibit the migration and invasion of HCC cells in vitro,and notably decrease the lung metastasis of HCC in vivo.Increased expression of E-cadherin and decreased expression of vimentin indicated that EMT was inhibited.Consequently,degradation of FAK through FAK PROTAC effectively suppressed liver cancer metastasis,holding significant clinical implications for treating liver cancer and developing innovative anti-neoplastic drugs. | XINFENG ZHANG SHUANG LI MEIRU SONG YUE CHEN LIANGZHENG CHANG ZHERUI LIU HONGYUAN DAI YUTAO WANG GANGQI YANG YUN JIANG YINYING LU | 2024 | Oncology Research2024，32，4： | 0 |
| 5 | Turning gas hydrate nucleation with oxygen-containing groups on size-selected graphene oxide flakes显示文摘Gas hydrate is a promising alternative for gas capture and storage due to its high gas storage capacity achieved with only structured water molecules.Nucleation is the critical controlling step in gas hydrate formation.Adding an alien solid surface is an effective approach to regulate gas hydrate nucleation.However,how the solid surface compositions control the gas hydrate nucleation remains unclear.Benefiting from the fact that the surface compositions of graphene oxide(GO)can be finely tuned,we report the effect of functional groups of size-selected GO flakes on methane hydrate nucleation.The carbonyl and carboxyl of GO flakes showed a more prominent promotion for methane hydrate nucleation than the hydroxyl of GO flakes.Surface energy,zeta potential,Raman spectra,and molecular dynamics simulation analysis were used to reveal the regulation mechanism of the functional groups of size-selected GO flakes on methane hydrate nucleation.The GO flakes with abundant carbonyl and carboxyl exhibited higher charge density than those enriched in hydroxyl.The negatively charged GO flakes can induce water molecules to form an ordered hydrogen-bonded arrangement via charge-dipole interactions.Therefore,the water molecules surrounding the carboxyl and carbonyl showed a more ordered hydrogen-bonded structure than those around the hydroxyl of GO flakes.The ordered water arrangement,similar to methane hydrate cages,significantly accelerated methane hydrate nucleation.Our study shows how the surface chemistry of solids control gas hydrate nucleation and sheds light on the design of effective heterogeneous nucleators for gas hydrate. | Huiquan Liu Changrui Shi Zherui Chen Shuai Wang Mingjun Yang Jiafei Zhao Cong Chen Yongchen Song Zheng Ling | 2023 | Journal of Energy Chemistry2023，，12： | 0 |
| 6 | Oridonin inhibits SARS-CoV-2 replication by targeting viral proteinase and polymerase显示文摘COVID-19 has become a global public health crisis since its outbreak in China in December 2019.Currently there are few clinically effective drugs to combat SARS-CoV-2 infection.The main protein(M^(pro)),papain-like protease(PL^(pro))and RNA-dependent RNA polymerase(RdRp)of SARS-CoV-2 are involved in the viral replication,and might be prospective targets for anti-coronavirus drug development.Here,we investigated the antiviral activity of oridonin,a natural small-molecule compound,against SARS-CoV-2 infection in vitro.The time-of-addition analysis showed that oridonin efficiently inhibited SARS-CoV-2 infection by interfering with the genome replication at the post-entry stage.Mechanistically,the inhibition of viral replication by oridonin depends on the oxidation activity ofα,β-unsaturated carbonyl.Further experiments showed that oridonin not only effectively inhibited SARS-CoV-2 Mpro activity,but also had some inhibitory effects on PLpro-mediated deubiquitinating and viral polymerase-catalyzed RNA elongation activities at high concentrations.In particular,oridonin could inhibit the bat SARS-like CoV and the newly emerged SARS-CoV-2 omicron variants(BA.1 and BA.2),which highlights its potential as a pan-coronavirus antiviral agent.Overall,our data provide strong evidence that oridonin is an efficient antiviral agent against SARS-CoV-2 infection. | Zherui Zhang Hongqing Zhang Yanan Zhang Qiuyan Zhang Qiaojie Liu Yanyan Hu Xiaoling Chen Jing Wang Yujia Shi Chenglin Deng Peng Gong Bo Zhang Xiaodan Li Bing Zhu Hanqing Ye | 2023 | Virologica Sinica2023，38，3： | 0 |
| 7 | Rational design of platinum(Ⅱ)complexes with orthogonally oriented triazolyl ligand with emission enhancement characteristics for cancer chemotherapy in vivo显示文摘The mitochondria are essential for tumorigenesis and have been regarded as important targets in cancer chemotherapy.Herein,the mitochondria-targeted platinum(Ⅱ)complexes have been prepared.The introduction of the triazole group with larger steric hindrance through post-click reaction converts the hybridization of carbon from sp to sp^(2),endowing the complexes with an orthogonally oriented ligand with restricted rotation and emission enhancement characteristics.Methylation of the triazolyl ligand has led to platinum(Ⅱ)complexes that can efficiently enter cancer cells and selectively accumulate in mitochondria,leading to significant enhancement in phosphorescence.In vivo anti-cancer investigations have demonstrated their distinct antitumor efficacy in substantial inhibition of tumor growth in breast cancer mice through dissipation of mitochondrial membrane potential,inducing apoptosis of tumor cell with negligibly systemic cytotoxicity. | Yeye Ai Zherui Zhang Yuexuan Fei Ruirong Ye Angela Sin-Yee Law Zong-Wan Mao Junqiu Liu Yongguang Li Vivian Wing-Wah Yam | 2023 | Science China Chemistry2023，66，10： | 0 |
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